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Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma
Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456124/ https://www.ncbi.nlm.nih.gov/pubmed/36077080 http://dx.doi.org/10.3390/ijms23179679 |
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author | Sasaki-Tanaka, Reina Ray, Ranjit Moriyama, Mitsuhiko Ray, Ratna B. Kanda, Tatsuo |
author_facet | Sasaki-Tanaka, Reina Ray, Ranjit Moriyama, Mitsuhiko Ray, Ratna B. Kanda, Tatsuo |
author_sort | Sasaki-Tanaka, Reina |
collection | PubMed |
description | Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease. |
format | Online Article Text |
id | pubmed-9456124 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-94561242022-09-09 Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma Sasaki-Tanaka, Reina Ray, Ranjit Moriyama, Mitsuhiko Ray, Ratna B. Kanda, Tatsuo Int J Mol Sci Review Alcohol is the one of the major causes of liver diseases and promotes liver cirrhosis and hepatocellular carcinoma (HCC). In hepatocytes, alcohol is converted to acetaldehyde, which causes hepatic steatosis, cellular apoptosis, endoplasmic reticulum stress, peroxidation, production of cytokines and reduces immune surveillance. Endotoxin and lipopolysaccharide produced from intestinal bacteria also enhance the production of cytokines. The development of hepatic fibrosis and the occurrence of HCC are induced by these alcohol metabolites. Several host genetic factors have recently been identified in this process. Here, we reviewed the molecular mechanism associated with HCC in alcoholic liver disease. MDPI 2022-08-26 /pmc/articles/PMC9456124/ /pubmed/36077080 http://dx.doi.org/10.3390/ijms23179679 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Sasaki-Tanaka, Reina Ray, Ranjit Moriyama, Mitsuhiko Ray, Ratna B. Kanda, Tatsuo Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title | Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title_full | Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title_fullStr | Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title_full_unstemmed | Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title_short | Molecular Changes in Relation to Alcohol Consumption and Hepatocellular Carcinoma |
title_sort | molecular changes in relation to alcohol consumption and hepatocellular carcinoma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456124/ https://www.ncbi.nlm.nih.gov/pubmed/36077080 http://dx.doi.org/10.3390/ijms23179679 |
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